A 55-year-old man presents with headache, neck pain and dizziness. See if you can answer the questions below by looking at images 1 through 3 before looking at the duplicate images with arrows (images 4 through 6).
Q1 – What is the salient finding on the presented MRI study?
(a) Cortical atrophy
(b) Dural venous thrombosis
(c) Pachymeningeal thickening
(d) Subdural hematoma
(e) Demyelinating plaques
Q2 – What is the most likely diagnosis?
(b) Bacterial meningitis
(c) Pseudotumor cerebri
(d) Intracranial hypotension
A1 – (c) Pachymeningeal thickening. The salient finding on precontrast images is bilateral and symmetrical subdural fluid collections and pachymeningeal thickening.
Cortical atrophy (a) is false since supporting findings of cerebral atrophy, such as sulcal enlargement and ex vacuo ventricular enlargement, are not present. Dural venous thrombosis (b) is false given that T1-weighted images demonstrate slightly increased signal in the sinuses, but flow void is confirmed on T2-weighted images. No dural thrombosis is evident. Subdural hematoma (d) is false because there is no evidence of signal alterations associated with blood products on T1- or T2-weighted images. Demyelinating plagues (e) is also false. There are scattered T2 and FLAIR hyperintensities in the white matter of bilateral frontal lobes. However, these lesions do not demonstrate typical septocallosal distribution of MS demyelinating plaques.
A2 – (d) Intracranial hypotension. Diffuse, smooth, supra and infratentorial enhancement of the thickened dura mater is a classical finding of intracranial hypotension. Often, veins compensatorily distend (image 4, green arrow). Such compensatory distention includes the dural venous sinus flow void (image 5, green arrow).
Sarcoidosis (a) and pseudotumor cerebri (c) are false. Sarcoidosis and other granulomatous diseases, including tuberculosis, Wegener granulomatous, and fungal disease, may produce dural masses and pachymeningeal enhancement, though granulomatous processes typically affect the basilar leptomeninges rather than hemispheric convexities. They are often “lumpy-bumpy”. Bacterial meningitis (b) is false given that it is associated with leptomeningeal enhancement, not isolated pachymeningeal enhancement. It may be thick and irregular. Patients are usually very sick. Metastasis (e) is also false. Metastases, particularly breast, prostate, melanoma and RCC, can present with pachymeningeal enhancement. However, in the absence of medical history, metastasis is unlikely. Furthermore meningeal carcinomatosis often involves the leptomeninges (pia arachnoid) and may be “lumpy-bumpy”.
As a note, transient pachymeningeal enhancement can also be seen after cranial surgery and uncomplicated lumbar puncture.
Q3 (BONUS) – Which is not a supporting image finding of spontaneous intracranial hypotension in this case?
(a) Decreased dimension of the suprasellar cistern
(b) Empty sella
(c) Venous distension
(d) Effacement of the basal cisterns
(e) Tonsillar ectopia
A3 (BONUS) – (b) Empty sella. Supporting imaging features of spontaneous intracranial hypotension (SIH) include all but empty sella. Empty sella could be seen with idiopathic intracranial hypertension (IIH), previously known as pseudotumor cerebri. In spontaneous intracranial hypotension, venous engorgement at the dura mater across the sella turcica could produce reactive hyperemia and increase in size of the pituitary gland. Other supporting findings of SIH include small slit-like ventricles (image 6, green arrows) bowing of optic chiasm, flattening of the pons against the clivus, dural thickening and intense enhancement with extrathecal cerebrospinal fluid collection. Retroclival venous engorgement (image 4, green arrow) is a useful sign on sagittal T1 MRI supporting spontaneous intracranial hypertension.
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